A wall defect is generally a hole in the wall of the tissue of a living animal, such as humans, or a hole in the wall of a container, tank, bag filter, or planar filter, tent, inflatable device, etc. In muscles or tissues of living animals, repairs have been accomplished by inserting an occlusion or septal closure device into the aperture or defect. Such devices include those taught by U.S. Pat. Nos. 5,334,217 to Das and 5,108,420 to Marks.
The Das patent describes a septal defect closure device, its use and method of assembly, where individual disks of a thin flexible material are supported by a super-elastic material and are used to occlude a wall defect. The disks are conjointly attached to one another at the center of the disk. The thin flexible material used in the Das patent can include nylon, polyester, polypropylene and polytetrafluoroethylene (PTFE) polymers. The super-elastic material is a NiTi alloy, such as nitinol.
The super-elastic material of the Das patent is formed into a frame having several legs and can assume geometrical configurations such as triangles, hexagons, circles, and stars. A membrane is wrapped around the legs of the frame. The loops between adjacent legs bias the legs outwardly, to form a concave membrane surface, which is maintained in a highly tensioned fashion.
The Marks patent describes an occlusion device that can be transported via a catheter in a compressed state. Once through the aperture to be occluded, the device is released and wires supporting two membranes are positioned on each side of the aperture. A domed or umbrella shaped configuration is formed and the support wires urge the membranes towards one another and the wall where the aperture is located.
These prior devices have numerous drawbacks. The support frames of the Das patent include resilient wire loops where leg ends of the frame meet and are attached to one another. The loops generally extend beyond the periphery of the membrane and can irritate or damage adjacent muscle or tissue.
Similarly, the exposed wires of the Marks device act as an irritant to tissue or muscle adjacent the aperture or septum. Here the bare sharp ends of the wire structure can further cause tissue erosion.
The Das and Marks patent devices use a membrane of conventional thickness that when folded over a wire add undesired thickness to the device. Additionally, the patents rely on peripheral membrane support which leaves the central occlusion covering portion of the membrane vulnerable.
In the Das patent design, each leg is provided with a bend at the middle of its length. This bend can add a tendency to the device to fold when the frame is sitting against a very flexible tissue and the membrane is pressurized by the blood. This may be the potential mechanism of failure as reported by Agarwal, et al. (1996). Agarwal, S. K., Ghosh, P. K. and Mittal, P. K., "Failure of Devices Used for Closure of Atrial Septal Defects: Mechanisms and Management," The Journal of Thoracic and Cardiovascular Surgery, Vol. 112, No. 1, 1996.
Finally, none of the previously available devices have provided a sufficiently small enough insertion diameter and/or collapsed flexibility. These limitations have restricted the utility and ease of use of such devices.
Thus, in view of the above, a need exists for a closure device that eliminates or significantly minimizes the traumatizing effect of existing closure devices. Further, a need exists for a device which is stable under physiological loading conditions when situated against the anatomical tissue structure. A need also exists for a defect closure device that is collapsible or compressible so that it may fit into a 9 F (9 French), preferably 5 F or 4 F or smaller catheter for deployment in a defect.
A need also exists for a closure device that is able to occlude or close wall defects in structures such as containers, tanks, tents, inflatable devices or filters without removing the structure from its environment of use. The present invention can meet these needs.